This is the conclusion to our case from last Saturday. I suggest reviewing the original case presentation before diving into the discussion here.

A 43-year-old female presents feeling like there’s a knot behind her sternum. It began suddenly just after eating lunch. This is her initial ECG:

There is apparent ST-elevation in leads V1â€“V3. The question remains, however, whether this ECG shows a STEMI or just early repolarization. Let’s look at the factors affecting our diagnosis:

The Story

At first glance this patient’s story doesn’t seem too impressive. It sounds like she might have a food bolus obstructing her esophagus or maybe even some esophageal spasm or heartburn, but it’s important to remember that our first priority in emergency medicine is to rule-out badness. In this case the most concerning diagnosis in play is acute MI.

Looking at her symptoms objectively: she experienced a sudden onset of retrosternal chest pain that radiates to her left scapula. The pain is constant with associated nausea.

In the absence of findings highly diagnostic of a food bolus (i.e. inability to swallow saliva or water), it doesn’t matter that her vitals are normal and she isn’t short-of-breath, diaphoretic, vomiting, experiencing arm or jaw pain, or any of the other secondary features we associate with an acute MI. The symptoms that are present should have us considering MI until proven otherwiseâ€”especially in light of her borderline ECG.

The ECG

So we’re going to manage this patient as a possible AMI from a prehospital standpoint. The question now is whether she is experiencing an ST-elevation myocardial infarction (STEMI)â€”requiring immediate reperfusionâ€”or if the ECG is non-diagnostic and she can be further evaluated in the ED.

Well, I can tell you that it is indeed a STEMI. The reasons?

There’s too much ST-elevation in V1â€“V3 for a 43yo woman.

The T-waves in V1 and V2 are slightly too tall.

The take-off of the ST-segment in V2 is slightly to steep.

There are clear reciprocal changes.

While the first three findings work together to increase our suspicion of STEMI, it is the last one that seals the diagnosis. That will be the most important aspect of our discussion but first…

The Elevation

Using the PR-segment as baseline and measuring at the J-point, there is 1.5 mm of elevation in V1, 1.5 mm of elevation in V2, and 1.1 mm of elevation in V3. According to the ECG criteria cited in the Third Universal Definition of Myocardial Infarction (which is used by the AHA in their STEMI guidelines), this ECG would just barely qualify as a STEMI with 0.15 mV in V1 (> 0.10 mV needed) and 0.15 mV in V2 (= 0.15 mV needed). V3 would not meet STEMI criteria with 0.11 mV (< 0.15 mV needed).

While it’s nice that the patient meets the formal criteria, ECG’s that fall close to the values above tend to produce a lot of false-positives and false-negatives. That doesn’t instill too much confidence if we’re more concerned with making an accurate diagnosis than simply meeting the minimum standard set by the guidelines.

Anyone who has been following the blog should realize that we don’t often invoke millimeter criteria in our discussions. In fact, except when I’m using Dr. Smith’s formula to differentiate STEMI from early repolarization, I haven’t felt the need to measure the actual amount of ST-elevation on an ECG in a few years. The whole reason I even mention it in this discussion is that, while there is measurable ST-elevation, the actual values don’t offer us much guidance. Even if you’re going to use the guidelines to define a “STEMI” in your region, in a case like this you’ll probably want to have more to go on than a measurement that just barely meets the formal (and arbitrary) cutoff.

Much more important is the morphology of the ST-segments and T-waves and the presence of reciprocal changes.

Reciprocal Changes

So about those reciprocal changes…

They are best seen in leads I, aVL, V5, and V6.

Lead I: There is about 1 mm of horizontal ST-depression. This is concerning but not a slam-dunk.

aVL: There is about 0.5 mm of ST-depression with an inverted T-wave. This is also worrisome but still non-diagnostic.

V5: There is about 0.5 mm of ST-depression. This is slightly less concerning but significant in light of the other findings.

V6: More important than the amount of ST-depression present, the morphology of the ST/T-wave here is markedly abnormal. This finding is certainly ischemic in nature here and, combined with the borderline ST-elevation in the right-precordial leads, confirms the diagnosis of STEMI.

In most situations you shouldn’t see an ST-segment that slopes downward into an upright T-wave like we do in V6 (though there are certainly exceptions; some cases of LVH with subtle strain come to mind). It is usually an ischemic finding. Sometimes that ischemia is just due to increased demand from an elevated heart rate, but that’s still ischemia and worth noting.

As a result, there are times this morphology might be non-diagnostic or of little concern, such as when it is due to subendocardial ischemia in a septic patient or even an unusual normal-variant.

The ST-depression we see here could be ischemic but there are no signs to suggest it is reciprocal to a STEMI. This patient ended up ruling-out for MI.

In the ECG above (from a different case), we see a similar morphology in V3â€“V6. It turns out, however, the patient ruled-out for acute MI (troponin-I 0.01 ng/mL x 3 (ref <= 0.04 ng/mL)). This pattern was also nearly identical to her baseline tracing.

The big difference from our case, however, is the lack of ST-elevation anywhere.

Here’s a more obvious anterior STEMI with that same reciprocal down-up ST/T morphology in V5, V5, II, III, and aVF.

Here’s another subtle STEMI (LCx culprit) with the same reciprocal morphology in V3â€“V6 and II, III, and aVF.

This is an exceptionally subtle MI with that down-up reciprocal morphology visible in leads III and aVF.

This is very similar to the last ECG except for the frankly inverted T-wave in III, but there’s still that down-up pattern in aVF.

Another subtle anterior STEMI. This time the down-up pattern is only seen in lead III. For more from this specific case check out our write-up here.

What if there aren’t reciprocal changes?

Well that just makes your job harder. Unfortunately lack of reciprocal changes, while a bit reassuring, in no way rules out a STEMI. If you’re worried about anterior STEMI but don’t see reciprocal changes, you should still be worried.

Early (hyperacute) anterior STEMI. If an EKG this impressive shows no reciprocal changes you can imagine how tough it can be to identify a more subtle anterior STEMI without reciprocals.

Subacute anterior STEMI with a culprit in the mid-LAD and no reciprocal changes visible.

Conclusion

Going back to our initial case; the patient first stopped in the emergency department where she had some labs drawn and a chest X-ray performed.

Her initial troponin-I on a current-generation assay (in the U.S.; not high-sensitivity) came back undetectable at < 0.01 ng/mL (ref <= 0.04 ng/mL). Thankfully an astute emergency physician recognized the significance of the patient’s ECG and activated the cath lab before that value returned. Had they waited for the troponin they would have been falsely re-assured as it was still very early in the patient’s MI and the level simply had not had time to appreciably rise.

I doubt this patient would have gone to cath if they knew her initial troponin was “negative.”

Cath revealed an acute lesion in the proximal LAD that was stented to good result.

Addendum: Dr. Smith’s Formula

Earlier in this post I mentioned Dr. Smith’s formula for differentiating anterior STEMI from early repolarization. I love the formula and have found it to be highly accurate but there’s a reason I didn’t use it here:

We aren’t allowed to!

You cannot apply the formula to ECG’s with possible reciprocal ST-depression (along with several other exclusions).

While it is tempting to use the formula because the abnormalities here are not impressive, the presence of any reciprocal changes precludes its use. Had we tried to use it (with values of 2.0 mm, 375 ms, 13.5 mm), it would have given us an output of 20.1. This is much less than the cutoff of 23.4 and would be falsely reassuring that the patient wasn’t experiencing a STEMI.

Dr. Smith’s formula is very, very useful (though not perfect), but it has to be used properly to work.

1 Comment

Nice case and GREAT discussion by Vince! There is really NOTHING to add to Vince’s thorough discussion â€” but perhaps it might be helpful to some to see how someone else ( = me) approached this case. Although said in slightly different words … the approach is essentially the same as Vince’s …
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BELOW what I wrote before reading Vince’s Answer:
… I agree with those stating transport to the PCI center while contacting ED staff and the Cardiologist On Call. Changes are subtle, but there clearly is more ST elevation (coved in shape) in lead V1 than should be seen â€” which in association with some ST elevation in V2,V3 + slight ST elevation in aVR + slight-but-real ST flattening/depression in leads I,aVL,V5,V6 â€” make this in my mind suspicious of acute LAD occlusion in progress until we can demonstrate otherwise â€¦ A follow-up ECG/stat Echo should tell the tale. Whether this ends up getting done in the ED on arrival vs in the cath lab is a judgment call (based on personnel, local procedure, etc.). P.S. Is this 43yo woman a smoker? (unless I missed it â€” I didnâ€™t see this noted in the history given â€¦) â€” in which case her relatively â€œyoung ageâ€ offers no â€œprotectionâ€ â€¦ Await follow-up from Vince â€”

Ken Grauer58 Year Old Male, Workout Worry@ Eli — I don’t see AFlutter. That is, I see no indication of regular atrial activity at a rate consistent with AFlutter. Instead, the rhythm is irregularly irregular without P waves = AFib at a controlled ventricular response. In my opinion, one doesn’t need Sgarbossa criteria here to activate the cath lab. So, yes the…
2018-09-13 02:09:24

Vince DiGiulioIs epinephrine harmful in cardiogenic shock?Sorry about that; I copied the quote from the article and my browser automatically changed the "μ" to an "m". Thanks for noticing, and thanks for pointing it out in the most passive-aggressive manner possible.
2018-09-12 16:45:26

Ken Grauer, MDElectrocardiographically Silent High Lateral STEMI EquivalentHi Tom. This is a great case — so NICE that you posted it for others to learned from. But as I commented several times when you sent this case around to our group — the T waves in V2,V3 are disproportionately peaked and transition occurs early (between V1-to-V2) — so the chest leads are NOT…
2018-08-14 08:38:03

Eli58 Year Old Male, Workout WorryAnybody else see the possibility of a LBBB or A-Flutter? I'm not sure if this will make any difference with the treatments but im just trying to interpret it first because if there is a LBBB then it does not meat Sgarbossa criteria and if it is A-Flutter that could explain the hyper acute T's…
2018-07-20 21:29:21